Abstract
Prior functional studies have shown that endocannabinoids (ECBs) in the NTS can prolong baroreflex inhibition of renal sympathetic nerve activity (RSNA). The prolongation was eliminated by NTS microinjection of bicuculline or gabazine, indicating that modulation of GABAergic transmission was involved. ECBs have been found to presynaptically inhibit GABA release in other CNS sites. If this mechanism is operative in the NTS, there should be co-localization of neural ECB receptors (CB1R) on GABA cell profiles in the NTS. This immunohistochemical study was therefore performed to identify the distribution of CB1R and sites of co-localization with GABA in the NTS. Transverse sections (20 μm) through the rat NTS were processed for immunofluorescent double-labeling of CB1R and GABA. Fluorescent labeling identified GABA-positive, CB1R-positive, and GABA/CB1R-positive neurons in the NTS. Immunostaining for CB1Rs was located throughout the extent of the cardiovascular NTS, with a dense network around the lateral borders of the tractus at more caudal levels and the medial subnucleus at more rostral levels. Labeling for CB1Rs was evident on both fibers and soma of neurons and colocalization of the CB1R with GABA was visible mainly on fibers in the NTS. The colocalization of CB1R on GABAergic neurons provides anatomical evidence supporting ECB modulation of GABAergic transmission in the NTS. Supported by VA Medical Research Funds.
Published Version
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